Cerebral edema is among the most common causes of morbidity and mortality from both acute cerebral infarction and brain tumor. Treatment with steroids or hypertonic infusions (urea, Glucose) is generally unsatisfactory, with rebound being a frequent complication of the latter. It is proposed to evaluate the treatment of such cerebral edema with hyperosmolar agents which dehydrate the brain but are not metabolized by it. Glycerol has a short half-life in the blood (less than 1hr.), is both metabolized by the liver and excreted by the kidney, and has not been shown to have a rebound effect on the brain. Glycerol has been shown to dehydrate the brain of normal animals, but its effects on brain electrolytes, brain osmolality, and extracellular space are not known. Similarly, neither the optimum effective dosage of glycerol nor its effects on renal function, acid-base balance or fluid balance are known. We initially evaluate the effects of glycerol on the brain of normal animals (dogs). Then, the effects of glycerol in animal models of acute cerebral infarction (cold lesion) and implanted brain tumor will similarly be evaluated, along with concomittant effects upon renal function and acid-base balance. Particular attention will be paid to the problem of rebound. In this manner, it is hoped to derive a rational therapeutic approach for treatment of cerebral edema complicating tumor and acute cerebral infarction.